Induction of human β-defensin-2 in pulmonary epithelial cells by Legionella pneumophila: involvement of TLR2 and TLR5, p38 MAPK, JNK, NF-κB, and AP-1

Legionella pneumophila is an important causative agent of severe pneumonia in humans. Human alveolar epithelium is an effective barrier for inhaled microorganisms and actively participates in the initiation of innate host defense. Induction of antimicrobial peptide human β-defensin-2 (hBD-2) by vari...

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Veröffentlicht in:	American journal of physiology. Lung cellular and molecular physiology 2010-05, Vol.298 (5), p.L687-L695
Hauptverfasser:	Scharf, Stefanie, Hippenstiel, Stefan, Flieger, Antje, Suttorp, Norbert, N'Guessan, Philippe Dje
Format:	Artikel
Sprache:	eng
Schlagworte:	Alveolar Epithelial Cells - drug effects Alveolar Epithelial Cells - immunology Alveolar Epithelial Cells - metabolism Alveolar Epithelial Cells - microbiology Base Sequence beta-Defensins - biosynthesis beta-Defensins - immunology beta-Defensins - pharmacology Cell Line Cells, Cultured Gene Knockdown Techniques Humans Immunity, Innate JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors JNK Mitogen-Activated Protein Kinases - metabolism Legionella pneumophila - drug effects Legionella pneumophila - immunology Legionella pneumophila - pathogenicity Legionnaires' Disease - immunology Legionnaires' Disease - metabolism MAP Kinase Signaling System NF-kappa B - metabolism p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors p38 Mitogen-Activated Protein Kinases - metabolism Recombinant Proteins - pharmacology RNA, Small Interfering - genetics Toll-Like Receptor 2 - antagonists & inhibitors Toll-Like Receptor 2 - genetics Toll-Like Receptor 2 - metabolism Toll-Like Receptor 5 - antagonists & inhibitors Toll-Like Receptor 5 - genetics Toll-Like Receptor 5 - metabolism Transcription Factor AP-1 - metabolism
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